Replicative activity of X-chromosome and autosomes of Drosophila melanogaster in autosomal hyperploids and the problem of dosage compensation.

Replicative behaviour of two hyperploid autosomal arms (2L and 3L) of D. melanogaster has been analysed by 3H-thymidine autoradiography. Results reveal that hyperploid autosomal arms (2L-trisomy or 3L-trisomy) replicate synchronously with other disomic non-homologous chromosome arms i.e. there is no asynchrony in the initial mid or late phase of replication patterns between the trisomic 2L or trisomic 3L and disomic arms, suggesting that the extra dose of an autosomal arm can not alter the inherent pattern of replication of that arm. Results further reveal that 2L-trisomy or 3L-trisomy does not impart any influence on X-chromosomal replication in either sex. It is suggested from these results that change in the genomic dose of autosome does not play any role in modulating the replicative organization of the autosomes, 2L and 3L. Thus, although a regulatory mechanism of autosomal dosage compensation does exist for Drosophila, the hierarchy of genetic programming of regulation for X-chromosomal and autosomal dosage compensation might be different. Neither hypertranscriptive activity nor faster replication pattern of the male X-chromosome is influenced by 2L- or 3L-trisomy.